MOD 1.1 - Cell Injury Flashcards Preview

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Flashcards in MOD 1.1 - Cell Injury Deck (40):
1

What can cause cell injury/death? (7)

- Hypoxia
- Toxins
- Physical agents e.g. temperature extremes
- Radiation
- Micro-organisms
- Immune mechanisms e.g. allergic responses
- Dietary deficiencies

2

What happens during hypoxia?

- Area/body is deprived of Oxygen
- Decreases the rate of aerobic respiration

3

What are the four types of hypoxia?

- Hypoxaemic Hypoxia
- Anaemic Hypoxia
- Ischaemic Hypoxia
- Histiocytic Hypoxia

4

Describe hypoxaemic hypoxia

Low arterial oxygen content

5

Describe anaemic hypoxia

Compromise in ability of haemoglobin to transport Oxygen

6

Describe ischaemic hypoxia

Interruption of blood supply

7

Describe histiocytic hypoxia

Oxygen can't be used due to disabled oxidative phosphorylation enzymes

8

Describe Ischaemia

- Loss of blood supply
- More serious as substrate as well as oxygen is lacking

9

What are the two immune mechanisms for cell injury? Describe them

- Hypersensitivity = Host tissue is injured after an over vigorous immune reaction

- Autoimmune = Immune system can't distinguish self from non-self

10

Give 3 effects of the decrease in oxidative phosphorylation and therefore decrease in ATP as a result of ischaemic hypoxia

- Activity of Na+-K+ pump decreases therefore more Na+ and H20 in the cell which causes swelling, blebbing and oncosis

- Increases amount of Ca2+ in the cell

- Increases rate of Glycolysis which decreases pH and Glycogen therefore causing nuclear chromatin clumps

11

Describe the effects of an increase in cellular Ca2+

Activates enzymes such as:
- ATPase
- Phospholipase
- Proteases
- Endonucleases

(Irreversible effects)

12

What can cause non-ischaemic injury?

- Extreme cold therefore leading to frostbite
- Free radicals

13

What is the fenton reaction?

Fe2+ + H2O2 ==== Fe3+ + OH- + OH. (free radical)

14

What is the Haber-Weiss Reaction?

O2- + H+ + H2O2 === O2 + H2O + OH. (free radical)

15

Give four mechanisms of protection against cell injury

- Enzymes e.g. Catalase, Superoxide Dismutase
- Free radical scavengers
- Storage proteins e.g. transferrin
- Heat shock proteins e.g. Ubiquitin

16

What are the reversible changes of cell oncosis that can be seen with electron microscopy? (4)

- Blebbing
- Swelling
- Clumping of nuclear chromatin
- Dispersion of ribosomes

17

What are the irreversible changes of cell injury that can be seen with electron microscopy? (4)

- Myelin figures
- Cell membrane defects
- Rupturing of lysosomes
- Pyknosis, karyorrhexis, karyolysis

18

What are the reversible changes of oncosis that can be seen with light microscopy?

Decrease in pink cytoplasmic staining

19

What are the irreversible changes of oncosis that can be seen with light microscopy?

- Pyknosis (nuclear shrinkage)
- Karyolysis (lack of nucleus)
- Karyorrhexis (nuclear fragmentation)

20

Define oncosis

Cell death with swelling, changes occur in injured cells prior to death

21

Define necrosis

Cell death in living organisms where the morphological changes occur after a cell has been dead for some time. Leads to leakage of cell contents

22

Define apoptosis

Cell death with shrinkage, happens due to a regulated intracellular program where the cell activates enzymes for its own nuclear DNA and protein degradation. Forms apoptotic bodies

23

Which is ATP dependent/independent, necrosis or apoptosis?

- Necrosis = ATP independent

- Apoptosis = ATP dependent

24

What are the 4 types of necrosis?

- Coagulative necrosis
- Liquefactive necrosis
- Caseous necrosis
- Fat necrosis

25

Describe coagulative necrosis

- Protein denaturation is greater than active protease release

- Forms a 'ghost outline' of cells

26

Describe liquefactive necrosis

- Enzyme release is greater than protein denaturation
- Enzymatic digestion of tissues
- Proteins lyse and dissolve

27

Where is liquefactive necrosis common and why?

- In the brain

- Lacks coagulative factors

28

Describe caseous necrosis

- Forms a structureless debris (no ghost outline)
- Looks like cottage cheese
- Closely associated with TB

29

Describe fat necrosis. Where is it most likely to happen?

- Destruction of adipose tissue
- Increases lipase therefore increasing lipolysis
- Fatty acids are released which react with Ca2+ therefore forming calcium salts
- Happens in pancreas

30

What is gangrene? What are the types?

- Clinical term for necrosis that is visible to the naked eye

- Dry necrosis = air exposure e.g. umbilical cord
- Wet necrosis = infection e.g. septicaemia
- Gas necrosis

31

What are the two types of infarction that cause necrosis?

- White
- Red

32

Describe the features of white infarction (3)

- No blood
- No haemorrhage
- Single blood supply

33

Describe the features of red infarction (3)

- Extensive haemorrhage
- Venous insufficiency or reperfusion
- Dual blood supply

34

What is the consequence of infarction and what does this depend on?

- Death
Depends on:
- Blood supply
- Speed of ischaemia
- Tissue involved
- Oxygen content

35

Name 3 molecules released by injured/dying cells and give their effects

- Potassium (Can cause heart to stop)
- Enzymes (time dependent i.e. small enzymes are first)
- Myoglobin (indicator of renal failure)

36

Give the two types of apoptosis

- Intrinsic
- Extrinsic

37

Describe intrinsic apoptosis

- Mitochondria plays the central role
- Increases permeability of membranes
- Leads to cytochrome C leakage

38

Describe extrinsic apoptosis

- Death ligands bind to receptors on CSM
- Directly activates caspases

39

Give 5 examples of abnormal intracellular accumulations

- Water and electrolytes
- Lipids e.g. cholesterol
- Carbohyrdates
- Proteins
- 'Pigments' e.g. tattoos, bruising

40

What are the mechanisms for abnormal accumulations? (4)

- Abnormal metabolism
- Changes in protein folding/transport
- Enzyme deficiencies
- Can't degrade phagocytosed particles

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